The Lumleian lectures for 1850 ... On the pathology and treatment of delirium and coma / [Robert Bentley Todd].

  • Robert Bentley Todd
Date:
[1850]
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Licence: Public Domain Mark

Credit: The Lumleian lectures for 1850 ... On the pathology and treatment of delirium and coma / [Robert Bentley Todd]. Source: Wellcome Collection.

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    in the situation of the shrunk part. A softening of a portion of the cerebral hemi¬ sphere will often cause a collapse of the convolutions above it, and thus space will be created for the accumulation of fluid. 3dly. I think it may be laid down that the accumulation of any large quantity of fluid in the ventricles, or the development of a tumor in the substance of either hemis¬ phere, or the formation of a clot of blood there, is incompatible with the existence of a surrounding subarachnoid fluid. The pressure from within displaces the sub¬ arachnoid fluid, and prevents the secretion of it. Thus, we never find the two fluids, intraventricular and subarachnoid, existing together in large quantity ; they may exist together in small quantity in shrunk, small, and ill-nourished brains, and more espe¬ cially where the defective nutrition chiefly affects the hemispheres and the convolu¬ tions. For these reasons I have long adopted the opinion that the effusion of a large quantity of subarachnoid fluid is a result— and a result probably of a conservative kind—of the shrinking or diminished bulk of the brain from some cause, and that in no case does the accumulation of fluid around the brain cause compression of that organ, nor can it be regarded as a cause of coma. Rheumatic and gouty coma.—Coma oc¬ curs in the course of rheumatic fever and of gout. The mode of invasion of the comatose state in these affections is very analogous to that of delirium, and very commonly follows that affection—always when it takes an unfavourable course. A patient may be going on well in rheumatic fever ; he, however, suddenly becomes rest¬ less and uneasy, and falls into a comatose state, in which he dies. The late Mr. Abemethy has referred to three cases of this kind which proved fatal, and he states that he found no abnormal condition of the brain. His words are—“ I may also mention, that I formerly examined the brains of three persons who died in a coma¬ tose state, in consequence of the metastasis of rheumatism. In these cases no morbid appearance was observed in the brain, ex¬ cept some slight marks of inflammation of the pia mater.” These slight marks were, no doubt, nothing more than some in¬ creased vascular turgescence of parts of the membrane. The following case shows that every form of cerebral disturbance, delirium, convulsions, and coma, may occur in rheu¬ matic fever without any lesion of the brain which can bo detected by ordinary means of observation. Martha Mitchell, ad. 34, was admitted on the 18th June, 1844, with rheumatic fever, the knees and ankles being the joints affected. On the 19th she became deli¬ rious ; and a few hours afterwards she had a convulsive fit, succeeded by coma and death. At the post-mortem examination the brain and its membranes were found pale, but otherwise healthy. There were marks of recent pericarditis. The occurrence of coma is more frequent in gout than in rheumatic fever, whilst de¬ lirium seems more frequently to occur in rheumatic fever. It is chiefly in the cases of chronic gout, in which the system is attacked pretty generally, that this state occurs, and the state of the kidneys is highly favourable to its development. Rheumatic fever differs from gout remarka¬ bly, as regards the extent to which the kid¬ neys suffer. Although in both diseases these organs are much disturbed, and exhibit a considerable departure from their normal mode of action, in gout they are apt to suffer much in their nutrition. They shrink to one half their natural size; the tubes lose them epithelium; serous cysts are developed; lithate of soda is found de¬ posited in the tubes of the medullary por¬ tion. In persons who have long been vic¬ tims of gout, whose joints are crippled, and the articular surfaces covered with a layer of lithate of soda, looking like plaster of Paris, this state of kidney is probably in¬ variably present; and it is in such cases that we may generally expect the termina¬ tion of gout by coma. Frequently the morbid state of the kidney is indicated by the presence of albumen in the urine, but it may exist without the escape of serum into the urine; the absence of that princi¬ ple from the urine is, therefore, no proof that renal disease does not exist. The following case illustrates this form of gouty coma:—A gentleman’s butler, about 50 years of age, had been the subject of several attacks of gout. He was admitted into the hospital in consequence of a copious effusion into one knee-joint; and his urine was found to be sufficiently copious, clear, and pale, with a small quantity of albumen, lie suddenly became comatose, and died: and on examination we found a copious effusion of fluid into one side of the chest, which must have taken place a few hours before death, as I had satisfied myself by auscultation that no such effusion existed on the previous day ; there were also very contracted kidneys ; and the brain afforded no signs of disease. It is possible, however, that sudden death by coma may take place where there is no evidence of the diseased state of the kidneys which I have described. A gentleman, set. 35, a very nervous
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